Why is it that giant tortoises typically live for 100 years but humans in the United States are lucky to make it past 80? And why does the life of an African killifish zip past in a matter of months?

I’ve often mused about the variability of life spans and I figure pretty much everyone else has too. But while editing the new issue of Stanford Medicine magazine’s special report on time and health, “Life time: The long and short of it,” I learned that serious scientists believe the limits are not set in stone.

“Ways of prolonging human life span are now within the realm of possibility,” says professor of genetics Anne Brunet, PhD, in “The Time of Your Life,” an article on the science of life spans. My first thought was, wow! Then I wondered if some day humans could live like the “immortal jellyfish,” which reverts back to its polyp state, matures and reverts again, ad infinitum. Now that would be interesting.

Also covered in the issue:

“Hacking the Biological Clock”: An article on attempts to co-opt the body’s timekeepers to treat cancer, ease jetlag and reverse learning disabilities.

“Time Lines”: A Q&A with bestselling author and physician Abraham Verghese, MD, on the timeless rituals of medicine. (The digital edition includes audio of an interview with Verghese.)

“Tick Tock”: A blow-by-blow account of the air-ambulance rescue of an injured toddler.

“Before I Go”: An essay about the nature of time from a young neurosurgeon who is now living with an advanced form of lung cancer. (The neurosurgeon, Paul Kalanithi, MD, is featured in the video above, and our digital edition also includes audio of an interview with him.)

The issue also includes a story about the danger-fraught birth of an unusual set of triplets and an excerpt from the new biography of Nobel Prize-winning Stanford biochemist Paul Berg, PhD, describing the sticky situation he found himself in graduate school.

This year’s most-read Stanford Medicine magazine stories were all about the heart, surgery and the immune system – the themes of this year’s three issues. The top 10 (as determined by pageviews on our website):

If you want to understand the human immune system, try studying humans – not mice. That’s what Mark Davis, PhD, urges in a special report on the immune system in the new issue of Stanford Medicine magazine.

“Inbred mice have not, in most cases, been a reliable guide for developing treatments for human immunological diseases,” Davis says in the special report, titled “Balancing act: The immune system.”

As the editor of the magazine, I wanted to feature a story that showed how human-focused immunology research plays out. So I was glad to learn that the center is in the midst of its largest study so far – one to figure out the cause of chronic fatigue syndrome. A team led by Stanford professor of infectious diseases José Montoya, MD, is looking for meaningful patterns in the components of blood samples gathered from 200 patients with chronic fatigue syndrome and 400 healthy subjects.

“It’s like dumping a hundred different puzzles on the floor and trying to find two pieces that fit,” Davis says in our story. We also have a video about a patient’s seven-year battle with chronic fatigue, from despair to recovery.

“My rendezvous with insanity”: a Q&A with Susannah Cahalan, author of Brain on Fire: My Month of Madness, her memoir of surviving an autoimmune attack on her brain

“The swashbuckler”: on look back to the early days of molecular biology when Mark Davis cracked one of the greatest mysteries of the immune system

The issue also includes an article on efforts at the VA Palo Alto Health Care System to use peer-support services to help veterans with post-traumatic stress disorder, and a story on the growing concern that biomedical research results are often erroneous and efforts being made to solve the problem.

It used to be “big hole, big surgeon” — but no more, according to Stanford’s chair of surgery, Tom Krummel, MD, who’s one of the surgeons featured in Stanford Medicine magazine’s report on surgery and life in the operating room, “Inside job: Surgeons at work.”

During his career of more than 30 years, Krummel has seen a massive shift from open surgeries to minimally invasive procedures — major surgeries conducted with tools that work through small openings.

“We do the same big operation. We just don’t make a big hole,” he said in the article leading off the report.

In the same issue, CNN’s chief medical correspondent, neurosurgeon Sanjay Gupta, MD, talks about why he’s “doubling down” on his support for medical marijuana.

As the editor, I’m biased — but I think it’s worth a read, along with the rest of the issue, which includes:

“Sculpting bones”: on lengthening a young girl’s leg using an external fixator — a device described both as draconian and as the perfect blend of engineering and art (Check out our animation by Lighthaus showing how the device works)

Why aren’t we all drowning in fat? Before talking with Mary Teruel, PhD, this question certainly never occurred to me. (On a personal level, though, I admit I’ve wondered about the opposite!) But after our conversation I saw why it’s such a good question — and how great it is that Teruel has come up with an answer.

Normally your body replaces about 10 percent of your fat cells a year, explained Teruel, a Stanford assistant professor of chemical and systems biology. Little by little, the old ones die, and new ones develop from flat, spindly precursor cells.

Teruel knew, based on her previous experiments, that the switch that triggers the conversion of precursor cells into fat cells is an “on-off” sort, not a dimmer which can be dialed up and down.

Here’s what’s going on in a little more detail: The switch controls the amount of PPAR-gamma in a cell. PPAR-gamma is a nuclear receptor protein that is the master regulator of fat-cell development. In precursor cells, the switch is in the “off-state” and there’s no PPAR-gamma in the cell, but when the cell senses a stimulus that can cause fat cell development, the switch flips to the “on-state” and the cell rapidly makes huge amounts of PPAR-gamma which then turns on hundreds of downstream genes that create a full-fledged fat cell over a period of up to 12 days.

So here’s what was puzzling Teruel: Every human has a large number of precursor cells that all sense the same stimulus, but rather than all converting at once to fat cells (causing us to “drown in fat”) for a given strong stimulus, only a few cells develop into fat cells at any given time, allowing a healthy, constant renewal of our fat tissue. What allows this slow, controlled renewal of fat cells, as well as prevents the unhealthy situation in which all fat cells would turn back into precursors when PPAR-gamma drops below the threshold needed to flip the switch on? If you can manipulate the rate fat cells mature, you could do a lot for obesity.
Experiments she did with postdoctoral researcher Robert Ahrends, PhD, and colleagues, explain, and provide clues about how to control the rate at which fat forms.

The answer, they discovered, has two parts. First of all, they discovered that the master fat-regulator switch has multiple layers of feedback. Teruel, who has a PhD in aeronautical engineering, explains that these multiple layers allow the body to control the rate of fat cell formation much as a pilot would control the pitch of an aircraft. Second, they found that not all precursor cells are alike — they vary in the quantity they carry of PPAR-gamma and other regulatory proteins.

This realization is a big deal. For one thing, it gives researchers new ideas for treating obesity and diabetes — so far, conditions that resist effective treatment without serious side effects.

“If you can manipulate the rate fat cells mature, you could do a lot for obesity,” she pointed out.

“This might be the heart of how you treat disease,” said Teruel. “We can’t just use one drug for treatment. Disease is more complicated than people think. It would be like trying to control an airplane and only being able to turn the rudder. This might work in a car or boat, but an airplane can move in three-dimensions, and a change in any one dimension affects the other two. Only controlling one dimension is a sure way to crash the plane.”

Teruel’s Stanford website has more info about her research as well as a striking depiction of a fat cell’s development.

They published the results of their studies on Friday in the journal Science (subscription required). They were supported by Stanford University New Faculty Startup Funds, the National Institutes of Health (grant P50GM107615), the German Research Foundation, and the American Heart Association.

This probably won’t grab as many headlines as the news of a smartphone that wakes you up with the sizzle and smell of bacon, but it should!

A team of Stanford scientists is using 3D printing to create inexpensive adapters that make it easy to use a smartphone and an ordinary examination lens to capture high-quality images of the front and back of the eye. And – what seems to me as just as important – providing a nearly effortless way to share those images.

“Think Instagram for the eyes,” said one of the developers, assistant professor of ophthalmology Robert Chang, MD.

This is a big deal because most primary-care doctors have no good way to see into patients’ eyes, and no easy way to share the images. The usual eye-imaging instruments are expensive and hard to use, and even ophthalmologists who have the equipment and know-how find capturing and sharing the images slow going.

“A picture is truly worth a thousand words… Imagine a car accident victim arriving in the emergency department with an eye injury resulting in a hyphema – blood inside the front of her eye. Normally the physician would have to describe this finding in her electronic record with words alone. Smartphones today not only have the camera resolution to supplement those words with a high-resolution photo, but also the data-transfer capability to upload that photo securely to the medical record in a matter of seconds.”

The scientists describe the adapters, currently dubbed the EyeGo, in two articles in the new issue (volume 3, issue 1) of Journal of Mobile Technology in Medicine. And you can read my story to learn more about the development process, including how Myung pieced together the first prototype (with plastic bits he ordered from the Internet and a few Legos), how mechanical engineering graduate student Alex Jais created the first printed model on his own 3D printer, and how residents Lisa He, MD, and Brian Toy, MD, are leading studies to test them out.

Those interested in using an EyeGo adapter for research or beta-testing can e-mail the team at eyegotech@gmail.com.

The heart is a paradoxical organ. It declares its presence with that distinctive thump thump, yet its moment-to-moment condition is really hard to decipher. But as I learned while editing the just-published Stanford Medicine magazine special report “Mysteries of the heart,” new technologies and research are making it easier to assess heart health and diagnose disease. With heart disease the No. 1 cause of death worldwide, that’s good news.

As I discovered while editing the new Stanford Medicine magazine report on childbirth, the placenta is a terribly important organ yet a big question mark for most people. To help demystify it we used a new kind of storytelling – an interactive simulation that allows you to observe and control the development of the placenta. It’s a companion to an article on the epidemic of the potentially fatal condition known as placenta accreta.

The producer, David Sarno, a former Los Angeles Times technology reporter and a 2013 John S. Knight Journalism fellow, built the simulation using the tools of video game design. It’s the first finished product of his start-up, Lighthaus, dedicated to creating interactive digital stories. If you’re curious about the placenta – or this new mixture of technology and storytelling – click on the image above to get to the video. (Note: To run the program you’ll need the Unity web player, which is free and downloads pretty quickly at the link.)

PubMed, the massive index of biomedical research articles, has begun an experiment: Enabling the posting of comments on the articles’ citations. This might not seem like a big deal, but in this case the comments system, PubMed Commons, is creating a buzz.

Some of the tweets following the Oct. 22 announcement: “PubMed Commons will change the way science works, but I predict a big impact on science bloggers as well” (@Neuro_Skeptic), “Science buzz and criticism gets a powerful boost” (@phylogenomics) and “Seriously get ready for a turbo-charged #PubMed (@AlbertErives).”

It was actually two Stanford professors – biostatistician Rob Tibshirani, PhD, and biochemist Pat Brown, PhD – who got the project rolling. I talked with Tibshirani for an article in Inside Stanford Medicine about the project’s beginnings and what he hopes it will accomplish. For starters, he sees it as a way for readers to note errors in the scientific literature in a place other researchers will see. But he also hopes it will generally expand scientific discourse and build community:

“Science can be lonely,” Tibshirani said. “Just having people talk about your work is nice. Sure it’s nice to have good comments. But it’s nice to have comments at all. At least someone cares enough to read your paper.”

For now, during this expanded pilot phase, only individuals who have published articles indexed in PubMed can make comments or see them. Tibshirani says he’s hopeful the leaders of the National Institutes of Health will decide to allow the general public to see the comments too. More on the how and why of the project as well as the quandary over anonymous comments (yea or nay) in the article.